Although the major action of racemic beta(2 )-agonists on the airways is relaxation of airway smooth muscle, these drugs have several other effects mediated through beta(2 )-adrenergic receptors expressed on other cell types. These additional actions of beta(2 )-agonists may contribute to the efficacy of beta(2 )-agonists in relieving asthma symptoms. beta(2 )-agonists inhibit plasma exudation in the airways by acting on beta(2 )-receptors on postcapillary venule cells. They inhibit the secretion of bronchoconstrictor mediators from airway mast cells and inhibit effects on release of mediators from eosinophils, macrophages, T-lymphocytes, and neutrophils. In addition, beta(2 )-agonists may have an inhibitory effect on the release of neuropeptides from sensory nerves. The effect of beta(2 )-agonists on mediator release from structural cells in the airways such as epithelial cells is uncertain. Despite all of these inhibitory effects on inflammatory cells in vitro, beta(2 )-agonists do not appear to reduce the chronic inflammation of asthma. Desensitization is more readily seen in inflammatory cells than in airway smooth muscle cells and may account for this discrepancy. Corticosteroids may increase expression of beta(2 )-receptors in inflammatory cells to overcome the desensitization in response to chronic beta(2 )-agonist exposure.